This invention is related to the decubitus ulcer disease, and in particular to an improved seat cushion for reducing the occurrence of decubitus ulcer disease.
Decubitus ulcer disease (pressure sores) is a secondary condition which frequently occurs in elderly patients, and others whose mobility is limited. Pressure sores are a growing problem for patients, and for health care providers. Twenty percent of all patients admitted to long-term care facilities arrive with pressure sores. An additional 12% develop new sores over each subsequent six-month period. 1.7 million patients developed bedsores in 1993. The cost to treat bedsores was estimated at 8.5 billion in 1993. The number of patients requiring treatment for bedsores, and the associated costs, can be expected to increase in the coming years as the number of persons over 50 years of age increases. Patients confined to wheelchairs may also experience pressure sores as well. The persistent and increasing problem of pressure sores has prompted investigation into their causes.
Kosiak, who is referred to as the father of modern pressure sore research, defined pressure sores as localized areas of cellular necrosis. From his studies with dogs, he concluded that ischemia resulting from supracapillary pressures was one of the main causes of ulceration. Pressure ulcers were the result of ischemic, neurophic, and metabolic factors. Ulcers almost always occur in the tissue that overrides a bony prominence. When pressure exceeds tissue capillary pressure, ischemic changes result in ulceration.
Kosiak found that very high pressure over a short period of time was just as dangerous for developing ulcers as lower pressure over a longer period of time. 70 mmHg over two hours caused pathologic changes in the tissues of dogs, while 500 mmHg for two hours caused pressure sores. Kosiak's work showed that degeneration of the tissue occurs simultaneously at all levels, including the skin.
In 1930 Eugene M. Landis published a report on the Micro-Injection method for determining the blood pressure in capillaries. The method consists essentially of cannulating single capillary loops by means of a micropipette immediately adjacent to the edge of the cuticle of health individuals. 125 people were tested at the arteriolar limb, which showed a range of 21-43 mmHg with an average pressure of 32 mmHg. Nineteen people were tested at the summit of the loop, which showed a range of 18 to 32 mmHg with an average of 20 mmHg. Ninety nine people were tested at the venous limb, which show a range of 6-18 mmHg with an average of 12.3 mm Hg.
Landis further tested these individuals to determine how the capillaries would respond under stress. Stress was introduced by five methods: 1) venous congestion and capillary pressure; 2) hyperemia of heat; 3) capillary pressure in the histamine flare; 4) capillary pressure during local cooling of the skin; 5) capillary pressure after injury of the skin. Capillary response to the stresses was a uniformed increase of pressure to combat the stress, which is better known today as a compensatory response. Landis concluded that human capillary pressure varies through much wider limits than had been previously supposed. These measurements became the reference points for later research in capillary occlusion, secondary to pressure.
Disdale used pigs to study the effects of friction on the tissue and their role in the development of pressure sores. He found that friction increased the susceptibility to the skin ulceration at a constant pressure of less than 500 mm Hg but that friction and repetitive pressure of only 45 mm Hg also resulted in skin ulceration. He found that decubitus ulcers were not totally the result of an ischemic mechanism but that friction was a factor in the pathogenesis of ulcerations because it applies mechanical forces in the tissues.
Research by Keane supported the fact that ischemic muscle necrosis, due to pressure, occurs before skin death. This finding was further supported by the research of Daniel, Priest, and Wheatley. These investigators found that the pathological changes were initially in the muscle, which then progressed toward the skin with increased pressure and/or prolonged duration.
Vistnes used pigs to study the pressure gradients from the bony surfaces within the tissue out to the surface of the skin. He believed that the highest pressure was located at the bony surface and that all ulcers started at the bone and worked out. A force exerted on a small-area internal bony prominence will produce a large pressure near the bone, while the same force transmitted to the larger area of the underlying skin with produce a smaller pressure.
Czerniecki studied the effects of increased skin loading on local circulation over both soft tissue and bone in humans. Three groups were studied: young, healthy populations; older healthy populations; and peripheral vascular disease populations. Transcutaneous oxygen tension was measured while pressure was applied to the electrode. Measurements were done on the amount of pressure applied, the amount of tissue displacement that took place, and the oxygen tension when local circulation was reduced to zero.
The work of all these researchers supports the conclusion that the subcutaneous tissue pressure is related to both the magnitude and direction of the externally applied load, and to the mechanical characteristics of the tissue. Therefore, when studying the effect of loads on tissue perfusion, it is desirable to measure both the applied load and the mechanical characteristics of the tissue.
As a result of this considerable body of research, it has been found that the primary factors associated with the occurrence of pressure sores are high, localized skin pressure, and friction forces on the skin. Skin pressure above a certain level impedes micro-circulation through the sub-cutaneous capillaries, and thereby impedes the flow of oxygen and nutrients to skin tissues. If the high skin pressure is not relieved, the skin break will down and pressure sores will develop, opening the body to infection.
Krouskop has researched the development of interfacing surfaces to reduce tissue stress in both sitting and lying positions. He evaluated the factors affecting the pressure-distributing properties of foam mattress overlays. He reported that mattresses support the human body through either the development of mechanical equilibrium between the body of given total weight or by resistance to deformation increasing with the depth of penetration of the supported body. Although the weight of the body deforming a mattress or overlay is constant, the applied pressure at the body/mattress interface changes with increasing area of contact. For this reason, minimum average pressure is achieved with maximum envelopment of the body by the mattress. Krouskop went on to compare different types of foams by use of a spherically shaped indentor to evaluate the load-bearing capacity of the foam and then compares these pressures to pressures generated in clinical settings. Krouskop understood that pressures can be reduced by increasing surface area contact, and arrived at 32 mm Hg as the maximum permissible pressure. Until now, it has been thought that the incidence and severity of pressure sores can only be reduced if high skin pressures of 32 mmHg are avoided.
As a result, there remains a need for an improved interfacing material which can be readily adapted for use on a seat cushion, and which can effectively reduce the occurrence of pressure sores.